Tag Archives: animal rights

Animal Rights Hacktivists

A handful of activists (maybe less) have begun to use digital means to take direct actions against those who are involved in animal research. All the hacks below involved gaining control of the website and either defacing the front page, or taking down the entire website. This is likely the actions of one or two lone activists, rather than the thousands involved in high profile distributed denial of service attacks (DDoS) – which were used to attack websites like the US Department of Justice in January.

On May 2nd 2012 the BiteBack extremist website reported that Riccó Alete, an Italian supplier of laboratory equipment, and SD Pellicceria, an Italian fur store, both had their websites defaced (apparently) by the notorious hacking group Anonymous.

Two days later, on May 4th 2012, Anonymous targeted  the website of Anlaids, an Italian non-profit organization which aims to tackle AIDS through information, research and funding.

However, this problem is not limited to Italy, or even Europe, on May 10th 2012 an American pet product company website was taken down by activists due to the activities of their sister-organization, Marshall BioResources, who supply equipment for laboratories.

Message left by hackers

Anonymous, for those who are unaware, is a loose collective of hackers from all over the world. Their effectiveness can be gauged from their high profile targets. They have (temporarily) crashed the websites of the Syrian Defence Ministry, the British Home Office, the US Department of Justice, Interpol and even the FBI.

Nonetheless, we should put this on perspective. As mentioned before, the number of anonymous members involved in the attacks on companies linked to animal research is very small – probably just one. The nature of anonymous is that anyone may carry out attacks in their name (it is a front group in this respect) and although they have a history of anti-establishment attacks, they do not have a history of targeting those linked with animal research.

Cheers

Tom

The Golden Goose Awards

Politicians sometimes deride research based on the what they perceive as being “silly” titles of federal funded grants.  If they spot a title that deals with “games”, for example, they may assume it deals with some sort of amusement of little value to society, instead of a deep, powerful branch of mathematics that describes the behavior of competing rational agents with much relevance to voting, economics, cooperation, and so on.  Animal rights activists also enjoy the hobby.  The latest example is IDA’s list of “ridiculous research” ,whose claims were sadly repeated by far too many news journalists who were clearly too lazy check if they were accurate.  There were some honorable exceptions, notably an excellent editorial entitled “When the facts ruin a good spin” in the Times Union, which discusses a project on the role of music as a conditioning stimulus for drug use ends with a statement with which we heartily agree:

What’s “ridiculous,” to borrow the press release’s language, is that we fall for it, over and over, egged on by politicians eager to score easy points. And what’s “wasteful” is the time and energy that could be so much better spent on something other than a cheap shot.”

Back in 1976 the House Committee on Appropriations asked the National Science Foundation “Why does the Foundation persist in supporting research whose results have no apparent value to the American people?“  The NSF responded in part that:

Basic research seeks an understanding  of the laws of nature  without  initial  regard  for specific  utilitarian  value. Ultimately, however, it  is of the  most important  practical significance, because in a broad sense it is the foundation upon  which rests  all technological development.  Applied research builds on the results of basic research, seeking detailed  information  about  a specific situation  whose general laws have  been  discovered by  basic  research.  The  final step  toward  utilization  of research-development is  the systematic  application  of knowledge to  the  design  of  end products. [...]

As we  increase  our  knowledge  of nature  and  mankind,  in order  to adjust  nature  to our survival, safety,  comfort and convenience, we must  depend  upon  scientific research  to clarify the  relationships  of many, many things.  Thus,  we study  atoms,  even  though  they  will never  be seen  by an  unaided  human  eye.  We study  stars  too  faint  to  be  seen without  a  telescope  and  with  wavelengths  which  can  only be  detected  with  radio  receivers  or  photographic  plates. To  understand  geology, we must  look  at  geologic formations  and processes in many  parts  of the world where different  conditions have existed.  To understand  more about the  phenomena  of life, we must  study  the  behavior  of viruses,  single  cells,  plants,  and  animals  of  many  species.

A book was compiled covering various areas of research with Isaac Asimov writing an essay defending the value of basic research.

Thus, it was with some surprise and delight that we read in the news about Rep. Jim Cooper (D-Tenn) understanding the value of basic research.  The Washington Post reports that:

On Wednesday afternoon, Cooper rose to the defense of taxpayer-funded research into dog urine, guinea pig eardrums and, yes, the reproductive habits of the parasitic flies known as screwworms–all federally supported studies that have inspired major scientific breakthroughs.

Together with two colleagues he created the Annual Golden Goose Awards to honor federally funded research  “whose work may once have been viewed as unusual, odd, or obscure, but has produced important discoveries benefiting society in significant ways.”

Studying dog urine, among other stuff deem crazy by animal rights cranks, led to major medical discoveries

The article goes on to describe how research on dog urine led to an understanding of the effects of hormones on the human kidney, how studies in the guinea pig led to a treatment for hearing loss in infants, and how studies on the screwworm led to the effective control of the a deadly parasite that targets cattle.  All these provide additional examples refuting the notion that learning about life processes from animals cannot yield knowledge applicable to human health.

The Golden Goose Award has the backing of the American Association for the Advancement of ScienceAssociation of American Universities (who in 2011 published a series of “Scientific Inquirer” articles skewering dubious politically-motivated attacks on basic science) and the Progressive Policy Institute, who are to be congratulated for this excellent initiative to highlight the importance of basic research.

At the press conference to launch the award Rep. Robert Dold told reporters that “When we invest in science, we also invest in jobs. Research and development is a key part to any healthy economy,” while  Rep. Charlie Dent (R-Penn.) added “It’s critical, and the federal government has an important role to play,” who went on to describe how injecting horses with snake venom might “seem peculiar” but led to the discovery of the first anti-venom.

Taking us, once again, to the concluding words of Asimov’s essay:

Unless we continue with science and gather knowledge, whether or not it seems useful on the spot, we will be buried under our problems and find no way out.  Today’s science is tomorrow’s solution — and tomorrow’s problems , too — and, most of all, it is mankind’s greatest adventure, now and forever.

Objections to the Marginal Case Argument

Scientists are often challenged with the so-called marginal case argument.

We are asked to spell out the criteria that make our experiments justifiable in animals but not in humans with comparable abilities and therefore comparable interests. These criteria, we are told, must be evaluated for each individual separately (so-called moral individualism). The resulting argument against animal research consists in pointing out that no matter what criteria are selected, it is always possible to find some humans (e.g., the senile, the cognitively impaired or the comatose patient) who should also be candidates for invasive research. According to this line of reasoning, logically consistency demands that we conduct experiments with these human patients along or instead of using animals.  If we are unwilling to do so, then we must be guilty of speciesism.

Same moral status?

Let me bring up a few objections to this argument.

First, it seems clear (to me at least) that the intrinsic properties of an individual cannot possibly be all that matters in assessing moral status of living beings.  If such properties were all that mattered, then we should feel comfortable granting a rock, a dead cat, and human remains the same moral consideration since they can all be classified as inanimate objects with no interests of their own.  And yet, while nobody will object to a child playfully kicking a rock, most will not feel comfortable with him kicking a dead cat for his or her amusement or using human remains in an art project for school.  The suffering such acts will inflict on others must count as well.  Thus, we must reject moral individualism. Once that premise is gone, the entire marginal case scenario falls apart.

Second, even if for the sake of argument one accepts moral individualism, the resulting moral theory is impractical. Are we prepared to evaluate every single individual we encounter in life to decide on his or her moral status?  Should we assess the cognitive abilities of the child now crossing the street? The dog walking with her? The squirrel that just rushed in front of our moving car?  On one hand, consistency demands that we do so, but applicability demands that we come up with a more practical approach. Indeed, our ability to function in daily life is aided by organizing the world into different categories (or kinds) of living beings and making broad assessments of their interests and moral status. Our brain’s ability to quickly recognize species membership facilitates this. It enables us to determine that the squirrel running in front of our car is a living creature and to swerve to avoid running it over—unless doing so would endanger the child crossing the street. In most situations, we can assess the interests of living beings based on the normal life of the members of that species. We have no need to assess the specific interests and moral status of this particular squirrel and this particular child.

Third, the marginal case scenario is nearly always posed by using an impaired human and a non-human animal, rather than a normal human and a non-human animal with super-natural abilities. Why? Because there is a clear difference between these two situations.  On one hand, should an ape appear in front of us, such as in Kafka’s “Report to the Academy”, speaking in fluent English, asking to be treated as a peer, it seems difficult to think we could refuse on any grounds, even if it represents an extraordinary case.  On the other hand, when human patients are impaired from their normal state, in most cases, we have no absolute certainty the condition is permanent.  A cure for Alzheimer’s or autism may possibly be developed in the future and their mental capacities restored.  Moreover establishing the lack of cognitive function with confidence may be more difficult than we have anticipated, with new studies showing that patients in vegetative state may retain some cognitive function. And, as I mentioned earlier, even in cases were science tell us there is no hope for recovery on the horizon, harming these patients would cause suffering in others that must also be taken into consideration.

Finally, there is also a scientific objection: Even if one were to accept on principle the suggestion by animal philosophers and activists that if we experiment on animals we ought to be experimenting on impaired human patients, that population would not be best suited for scientific studies. Patients with pre-existing conditions have a wide range of abnormalities and individual differences that would make it extremely difficult to conduct properly controlled scientific studies.  Thus, in addition to moral considerations, there are valid scientific reasons to reject the proposal of using impaired humans rather than animal subjects in most studies.

Good, bad, useful? Reflections on animal models for Parkinson’s disease research

Parkinson’s disease is a relentless, ruthless neurodegenerative disorder that often strikes in the early “golden years”, around 60 years of age, but sometimes much earlier.  It progressively robs its victims of every capability that makes life enjoyable, from their ability to move, talk, eat by mouth, and in the worst cases, decreasing their cognitive abilities.

In the sixties, pioneering work in animal models, primarily rats, led to the discovery of a “pill” that transformed the lives of many patients by restoring their ability to move and allowing them to perform daily tasks, often continuing to work, travel, and to enjoy sports and family time.  In research that earned him a Nobel prize many years later, Arvid Carlsson and colleagues reproduced in these rats the main chemical deficit that exists in patients, and found that administration of l-dopa (sinemet) could greatly improve the motor deficits of PD patients.

Subsequent work, always based on generating a “model” of the disease in animals by destroying the neuronal cells that also die in patients, have led to refinement of this treatment; additional advances have led to surgical methods (deep brain stimulation) that further improved quality of life for many patients.

Why should we continue to use animals to study this disorder?

First, as any patient will tell you, the available treatments do not work on all the symptoms they experience, such as depression, sleep disorders, and digestive problems that plague their lives often even more deeply than their motor disorders. Second, the current treatments do not cure the disease, and their benefits do not last forever. In time, the treatments progressively lead to side effects, for example uncontrolled movements or spasms that leave the patient to chose between not moving at all or moving too much. Today’s medications do not stop the progressive loss of nerve cells in the brain, which will ultimately lead to disability and death.

A real treatment for the disorder will have to address its root cause and stop its process, perhaps even reverse them. This is where a lot of confusion on the utility and value of the animal models arises. In the press and even the scientific literature there are statements expressing concern that there is “no good model” of Parkinson’s disease, and sometimes that existing models are useless because some drugs that work in animals fail in the clinic.  It is a complex issue that is a source of debate among scientists and lay people alike. However, one has to examine the roots of the problem.

Models are only as good as our understanding of a human disease at a given time. Science is an evolving process and so are our models of disease. There was a time when we did not understand why some people would die from blood transfusion and others did not, because blood types had not yet been discovered. In the case of Parkinson’s disease, we have known for about a century which cells die in the brain of patients but we still do not know why. The early models, those that led to the major breakthroughs in treating some of the symptoms of the disease, reproduce this loss of cells but do not address its mechanism. We now know more about this mechanism because of research on the causes of rare cases of the disease that have a genetic component and run in families. We also know that even though most cases of Parkinson’s disease do not have a clear genetic component, the mechanisms may be the same. New understanding has led to a new generation of models, in which defective genes are introduced in mice to reproduce the mechanisms thought to cause the disease in people.

GM mice help to uncover the processes of Parkinson's disease. Image courtesy of Understanding Animal Research.

Are those models perfect?

No model is perfect. No model can be expected to reproduce all the symptoms that occur in patients. Even if similar, the brain and nervous system of mice are not identical to those of a human, who walks on two legs, not four paws, and can live up to a hundred years rather than two. Yet, a lot of the general functions that are affected by the disorder in humans are present to some extent in the mouse model.

More importantly, only in an animal can one examine the very beginning of the disease process. Many studies in humans have now shown that diseases like Parkinson’s begin to affect a person’s body decades before they even know it. The disease causes subtle changes that are not even perceived as abnormal but have long-term consequences, just as a minute water leak can over years rot a wooden beam and lead to a roof collapse. As the disease progresses, it can manifest itself with minor troubles, so unremarkable that they are not recognized as related to Parkinson’s disease, for example problems with sleep and smell, that are very common and have many different causes.

Thus, in a human, we will never be able to understand the beginning of the disease, the water leak, because we do not know in which individuals they are occurring. This is where animal models are the most useful. By reproducing anomalies, such as the overexpression of the protein alpha-synuclein, that cause the disease in people, we can study the mechanisms from the beginning and find ways to stop the damage as early as possible.

Why then are people writing that animal models of Parkinson’s disease did not accurately predict whether a new treatment can be effective in patients? For one thing, those drawbacks were largely based on old models, which were – and still are – useful for some things (developing treatments for symptoms and evaluating new approaches to restoring lost function such as gene therapy) but were only minimally productive in developing treatments to halt the development of Parkinson’s disease because of our limited knowledge of mechanisms at the time.

Will the new models be better at predicting drug efficacy in the clinic? It is too early to tell because none of the new compounds developed and currently being tested in these models has yet been tested in patients. Should these animal models be replaced by computer modeling of the disease?  Probably, but this is years in the future. The science of modeling all the molecular interactions that take place within a cell, and of all the connections this cell establishes with other cells in a complex organism in a way that could illuminate a disease process and make sound predictions leading to effective treatments is in its infancy. In the meantime, patients are diagnosed, grow worse, and die every day.

We cannot wait. Just as previous models, although imperfect, led to transforming discoveries that bought years of functioning to patients who otherwise would have been locked in a chair and condemned to an early death, the new models continue to lead every day to discoveries that bring us closer to an effective treatment. Nothing can replace them at the moment.

Marie-Francoise Chesselet, M.D., Ph.D.
Charles H. Markham Professor of Neurology
University of California, Los Angeles

A Brief History of Deep Brain Stimulation

An on-going campaign against the use non-human primates to study Parkinson’s disease (PD) at the University of British Columbia prompted me to summarize some basic facts about the work and the history of a successful therapy was developed.

Why is the work done?

In the U.S. alone there are between 500,000 and 1 million people living with PD, with about 50 to 60 thousand new diagnoses every year.  The National Institutes of Neurological Disorders and Stroke (NINDS) estimates the cost to our society is at least $5.6 billion, including both direct medical expenses and indirect costs from lost income, disability payments and so on.  Moreover, the emotional toll of Parkinson’s on patients and families is enormous.

One of the most successful therapies developed for PD  involves the electrical stimulation of deep structures within the human brain — so called deep brain stimulation (DBS).  The technique works remarkably well for some patients.

How was the method developed?

Back in 1983 Langston and colleagues reported on a clinical case study of four patients that developed Parkinsonism after illicit drug use.  Analyses of the drugs they had taken via mass spectroscopy revealed primarily MPTP, but there were also traces of MPPP. They suggested MPTP might be the most likely culprit and suggested that:

“Given the pathologically studied case, the relative purity of the clinical syndrome seen in our patients, and its remarkable clinical resemblance to Parkinson’s disease, the drug [MPTP] may be of value in producing an animal model of Parkinson’s disease.”

In other words, a group of clinicians studied a handful of human patient cases, identified a potential link between MPTP toxicity and the development of PD, and proposed to follow up with animals studies.

In 1983, Burns and colleagues follow up on this idea by trying to replicate the disease in monkeys.  Indeed, intravenous administration of MPTP caused the animals to develop rigidity, postural tremor, eyelid closure, and many other symptoms of Parkinsonism.  Moreover, their symptoms could be relieved by the administration of L-dopa, exactly as it was the case with the Langston et al patients. The animal model also allowed them to characterize the selective destruction of dopaminergic neurons in the subtantia nigra and a marked reduction in the dopamine content of the striatum.  They offered MPTP treated monkeys as a model to explore therapies for PD.  How many animals were used?  Twelve.

Although these anatomical studies shed light into the brain areas that might be involved in PD it was unclear what functionally was causing the observed symptoms.  Subsequent work by Mitchell et al (1989) using single unit recordings and lesion studies in monkeys pointed to increased activity in the subthalamic nucleus (STN) as generating motor abnormalities.  How many monkeys were used?  Eight.

A natural question arose from these studies.  Would suppressing the activity of these hyperactive neurons help in alleviating the symptoms of the disease?

Two studies showed that lesions of the STN could reverse the effect of Parkinson symptoms in the monkey MPTP model, with studies by Bergman et al (1990) and Aziz et al (1991).  These studies not only began to dissect the functional connectivity within the basal ganglia-thalamocortical circuit, but also offered evidence that inactivation of the STN could work as a potential therapy for Parkinson’s.   How many monkeys were used in these two studies?  Four.

Shortly after, Benazzouz et al (1993) showed that instead of lessoning the STN one could use high frequency stimulation of the STN to alleviate the symptoms in MPTP treated monkeys.  Supposedly, the high frequency stimulation suppresses the activity of these cells acting as a “virtual lesion”.  How many monkeys were used here?  Two.

Indeed, Limousin et al (1995) successfully applied this method in three patients and concluded:

“In this study, bilateral subthalamic nucleus stimulation improved akinesia and rigidity in three patients with Parkinson’s disease.  This is in agreement with the results obtained in monkeys with MPTP-induced parkinsonism by lesions or stimulation of the sub-thalamic nucleus.”

Number of humans used?  Three.

And to dispel any remaining doubts he writes in a recent review that:

“The knowledge of the functional changes of basal ganglia activity in the parkinsonian state as it emerged from extensive experimental studies on animal models has provided the theoretical basis for surgical therapy in PD. The 6-hydroxydopamine (6-ODHA) rat model and the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) primate model of PD provided powerful research tools for uncovering the pathophysiology of changes in functional basal ganglia activity in PD.” 

And finally one may ask, ho many human patients have benefited from this type of work?

The answer is 80,000 and counting.

What do these patients think of such studies?

Here is one — please listen to him carefully.

And if you truly want to learn more here are some extra resources:

SfN brain briefing on PD discoveries.
The Michael J. Fox Foundation
Information from National Institutes of Neurological Disorders and Stroke.
Information from Understanding Animal Research.

Understanding Adverse Drug Reactions (ADRs)

Looking through some animal rights websites and forums I see the same misconceptions come up again and again on the subject of animal research. The first questions can be paraphrased thus:

“If animal research advances medical science, how come when the animal experiments end and the products go to market, the humans experiments begin?”

There are several reasons why we require both animal and human clinical trials. Animal research plays three roles in research – understanding, development and safety testing – you need to understand how a biological system or a disease works, then you need to model pathologies in order to develop a treatment, and finally you need to ensure that this new treatment is safe.

1. Understanding – we use a variety of techniques to understand the body and its pathologies – we might use cell cultures to understand individual reactions, population studies to find environmental causes, or fMRI to understand effects in the brain. However, it is likely that some animal studies will be needed, or relied upon, at this stage. For instance, if you want to study how the heart works you need a fully functioning one to use – cadavers are no good. Few humans would allow a researcher to open them up and run tests to see how a healthy heart works – so for this we need animals. If you want to understand how a disease works you need to see from the start what happens when a healthy body is attacked by it. It would be unethical to start infecting humans with a disease you couldn’t yet cure – so we use animal models to try and learn how a disease works – how it spreads through the body, what secondary and tertiary effects it has etc.

2. Development – now that we have some pathology in the body we understand we now need to try and treat it. Using all we know about the body, learned from both animal and non-animal methods, scientists can hypothesize as to approach needed in treating – will surgery solve the problem, do we need to give some kind of antibiotic, or is something different required? In this development stage we need a model that can be used to treat. The problem with using humans is that some of the approaches to treatment may be quite novel and we do not want to harm a human. Scientists do not have a 100% clear understanding of how a human body works (not even close) and so it can be difficult to know what the effects, or side effects may be to a treatment. To solve this, we use animals to model the disease. In some cases the treatment may come directly from the animal – for instance Herceptin, a drug for breast cancer, is a (artificially) humanized version of a mouse antibody. Insulin, a lifesaving treatment for Diabetics, was originally made from dogs.

3. Safety Testing – when a research institution comes up with a new treatment it must undergo stringent tests to ensure its safety. Before it is let anywhere near humans it must first pass animal tests to check that it’s not going to cause harm to humans in early stage clinical trials. Animal tests are not there to decide whether a drug is completely safe for market, it is there to check that the drug is safe enough for small, controlled clinical trials. Many, many drugs do not pass these animal tests – they are deemed to dangerous or ineffective to be moved on to clinical trials. To see the clear success of animal safety tests we should consider how rare it is that something goes wrong in a Phase I clinical trial (the first time it is tested in humans) – the only recent disaster Phase I was the 2006 Northwick Park  (in the UK)  disaster of TGN1412. Contrary to activists later claims that profits outweigh law suits, TeGenero, the company responsible for TGN1412, went bankrupt following the disaster. Some scientists have argued that TGN1412 was passed too quickly from animal tests to clinical trials – neither the in vitro nor the animal preclinical studies underaken by TeGenero predicted the adverse response in human volunteers. An official report published by an expert scientific group brought together by the Department of Health mad a series of recommendations to improve the effectiveness on both in vitro and animal tests used to evaluate the safety of new medicines, particularly biological molecules such as TGN1412 which have novel mechanisms of action.  The reports authors acknowledged the importance of animal research to the development of new medicines, writing that:

Animal studies taking due regard of the three ‘Rs’, (refinement, reduction and replacement of animals in testing) remain necessary for many aspects of pre-clinical development of novel agents including testing of ‘off-target’ and ‘on-target’ toxicity and understanding the fundamental biology relevant to a new medicine and its target molecules in the human. Most, if not all, new medicines arise from biological insights gained from well-designed animal studies. The key point we want to make is the importance of deciding what can be learned from animal studies in the pre-clinical development of a new medicine, and what limitations there might be when it comes to predicting the response, and dose-response relationship, in humans.

Even when the drug has passed animal tests to declare they are safe to begin human testing there are many questions – what is the correct dosage? Will the drug be effective in humans? Animal testing will suggest how a drug will react in humans – but it is not a perfect model – just as a drug will react differently in different people. What are the side effects? Some of these may have been discovered in animal tests (and been considered acceptable), but there may be some human only side effects. For this reason we need both the human and animal safety tests before we can release a drug onto the market. We should remember that no drug is released onto the market on the basis of animal tests – but rather on the results of the clinical trials (in humans) which follow.

If animal safety tests work why is it that people still die from adverse side effects?”

Many animal rights activists have fallen into the common mistake of believing that Adverse Drug Reactions (ADRs – essentially “negative side effects”) can be blamed on animal research. The first clear point is that EVERY drug has ADRs. Look in the leaflet that comes with any medicine and you will see things like “may cause drowsiness” – this is an ADR. This does not mean you WILL get this side effect, but because everybody has slightly different DNA, they can produce slightly different effects from a drug. Now lets revisit an earlier point – I’ll put it in bold – no drug is released onto the market on the basis of animal tests – but rather on the results of the clinical trials (in humans) which follow. The implication of this is that even human research cannot ensure every drug is 100% safe. Clinical trials might include several thousand people and show no statistically dangerous effects, but if 80 million prescriptions are given (as was the case for Vioxx) and a fatal side effect affects 1 in 400 (Vioxx again), then this may still cause a tragedy.

Furthermore, many ADRs are known and accepted, even before a drug finishes – or even starts – clinical trials.  Chemotherapy can carry a risk of potentially serious side effects, up to and including death – yet many more cancer-sufferers are likely to die without it – so the risk is worth it. So can we measure the potential harm that drugs are causing? Well between 1997-2000 around 150 novel drugs were approved by the FDA (and many hundreds of non-novel ones). Over the same period only 10 were withdrawn due to potentially dangerous side effects (under 7%).

Side effects of inhaler use can include sore throats and oral thrush

A further point must be made on the scale of prescriptions. The more people that take a drug, the more likely that ADRs will occur, even when it only affects a tiny proportion of the population. Let us consider the following list of medications made possible by animal research. Every year in the US there are:

  • 1,500,000 prescriptions for Erythropoietin, used to treat anaemia
  • 34,000,000 anticoagulants dispensed, this can treat blood clots which are associated with many causes of death e.g. Pulmonary Embolism
  • 95,000,000 prescriptions for asthma inhalers
  • 150,000,000 prescriptions for antibiotics, used to treat infection – the most common of which is Penicillin

Now, sadly, some people have had fatal allergic reactions to asthma medication – but we shouldn’t be throwing the baby out with the bathwater – this medication helps (and often saves) the lives of 15 million asthma sufferers in the US (which disproportionately affects children). However, if there is an ADR associated with asthma medication which affects, say, 1 in 1 million people, then 15 of those asthma suffers may end up negatively affected by the medication.

Overall, the huge majority of us who take medical treatments have no side effects at all. For more serious diseases such as cancer, we go through the treatment aware that the side effects are better than consequences of neglecting treatment. ADRs are not something which are going away any time soon, but to blame animal research for their existence shows a fundamental misunderstanding of what they are.

Tom Holder

A welcome end to random-source dog and cat dealers

The National Institutes of Health has announced that starting October 1, 2012, NIH funds may no longer be used to buy cats from Class B dealers. A similar prohibition in the purchase of dogs from Class B dealers takes effect in 2015.

Although dogs and cats constitute only small percentage of research animals, they have been used in American biomedical research for over a century for studies of cardiovascular and neurological diseases, and for other areas of research including recent studies that led to a gene therapy for the eye disease Leber’s congenital amaurosis, whose success was reported widely last week.  The use of these animals is tightly regulated by the Animal Welfare Act, and they are only employed for studies where lower species do not provide adequate models.

Class B dealers are individuals licensed by the USDA under the Animal Welfare Act to resell animals they did not breed themselves. Class A dealers are breeders who do raise the animals themselves. Class B dealers may purchase dogs and cats from sources such as municipal pounds, from individuals who bred and raised the animals, and from other licensed dealers. They are required to keep records on where they got each animal and to hold pound animals for a minimum period so that if an unwanted animal was actually a stray, the owner has time to reclaim it.

Animal statistics in 2010 (US data) - Dogs account of 0.25% and cats 0.08% of the total number of animals used.

Class B dealers used to provide a large number of cats and dogs for research because they were virtually the only source for older animals and for some breeds. Regrettably, some Class B dealers used practices that violated the Animal Welfare Act both in terms of how they acquired animals and how they treated them.  The National Academies of Science studied the specific areas of science where Class B dogs and cats were being used and concluded that NIH could develop alternate supply mechanisms to replace them. NIH decided the best way to facilitate the transition was to provide an initial outlay of funds so that Class A dealers could begin raising older dogs of the breeds required for scientific research. It is expected that these breeders will be able to produce the necessary animals by 2015.

After October 1, 2012, NIH-grant supported research can only use cats from the following sources: Class A dealers, privately owned research colonies, or client owned animals, such as animals that participate in veterinary clinical trials.  The same policy will apply to dogs in 2015 when the Class A breeding program is in full swing.

The transition of NIH-funded research away from the use of Class B dogs and cats is an example of how measures can be taken to correct ethical problems regarding the treatment of animals.  When ethical concerns exist, thoughtful and deliberate steps can address those concerns, while preserving important biomedical research projects.

Bill Yates and Alice Ra’anan.

Bill Yates is the Chair of American Physiological Society Animal Care and Experimentation Committee. Alice Ra’anan is Director of Science Policy for the American Physiological Society. The views expressed above are exclusively those of Bill Yates and Alice Ra’anan and do not necessarily represent those of their employers.